Evidence map›Paper›PMID 40493023›Full record

ArticleMolecular oncology2025

Cytomegalovirus infection is common in prostate cancer and antiviral therapies inhibit progression in disease models.

Johanna Classon, Moa Stenudd, Margherita Zamboni, Kanar Alkass, Carl-Johan Eriksson, Lars Pedersen, Alrik Schörling, Anna Thoss, Anders Bergh, Pernilla Wikström and 4 more

Abstract read
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Johanna ClassonDepartment of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.ORCID 0000-0003-0392-7605
Moa StenuddDepartment of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.
Margherita ZamboniDepartment of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.
Kanar AlkassDepartment of Pathology and Oncology, Karolinska Institutet, Solna, Sweden.
Carl-Johan ErikssonDepartment of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.
Lars PedersenDepartment of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
Alrik SchörlingDepartment of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.
Anna ThossDepartment of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.
Anders BerghDepartment of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden.
Pernilla WikströmDepartment of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden.ORCID 0000-0002-6347-1999
Hans-Olov AdamiDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
Henrik Toft SørensenDepartment of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
Henrik DruidDepartment of Pathology and Oncology, Karolinska Institutet, Solna, Sweden.
Jonas FrisénDepartment of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.ORCID 0000-0001-5819-458X

Funding

CancerfondenKnut och Alice Wallenbergs StiftelseStiftelsen för Strategisk ForskningVetenskapsrådet
6 · The paper itself

Abstract

Metastatic prostate cancer is incurable, and new therapeutic targets and drugs are urgently needed. Viral infections are associated with several cancer types, but a link between viruses and prostate oncogenesis has not been established. Only recently, an association between human cytomegalovirus (CMV) seropositivity and increased risk of prostate cancer mortality was demonstrated. Here, we show that CMV infection is common in the normal prostate epithelium and in prostate tumor tissue, with 70-92% of tumors being infected. Additionally, we report that commonly studied prostate cancer cell lines are CMV infected. Loss-of-function experiments demonstrate that CMV promotes cell survival, proliferation, and androgen receptor signaling, identifying it as a therapeutic target in castration-sensitive and castration-resistant prostate cancer. Several anti-CMV pharmaceutical compounds in clinical use inhibited cell expansion in prostate cancer models both in vitro and in vivo. We conclude that CMV is common in prostate cancer, promotes core prostate cancer cell programs, and can be inhibited by well-tolerated drugs. These findings motivate investigation into potential clinical benefits of CMV inhibition in the treatment of prostate cancer.

Indexed as

Antiviral AgentsCytomegalovirusCytomegalovirus InfectionsProstatic NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease ProgressionHumansMaleMiceReceptors, AndrogenAntiviral AgentsReceptors, Androgenantiviral treatmentcancer therapycytomegalovirusprostate cancer

Identifiers

PMID40493023
PMCPMC12591316

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.